Wednesday, February 25, 2009

This patient is 38 years old with hyperlipidemia. He was at the gym when he had the onset of chest pain. EMS was activated and recorded the following ECG (scanned from a prehospital ECG, so the quality is not perfect):

Notice the small Q wave in V1 followed by a very large R-wave, with a prolonged QRS. There is a wide S-wave in V6. Thus, there is right bundle branch block, which should never (unlike Left BBB) have any ST elevation. But here there is a large degree of ST elevation in V2-V6, I, and aVL. RBBB in acute STEMI has a very high mortality.

The paramedics activated the cath lab from the field.

The patient had 2 ventricular fibrillation arrests during transport, but was immediately defibrillated both times, and was awake in the ED, when the following ECG was recorded:

The ST elevation has mostly resolved on this ECG, and were it not for the arrest and the prehospital ECG, this would not be a slam dunk diagnosis. There is still ST elevation in I and aVL, but it is subtle. There are abnormal T waves in V2-V4, with straightening of the ST segment which is typical of hyperacute T waves.

Angiography revealed a very tight LAD stenosis with some flow (confirming the reperfusion that we see on the ECG). A stent was placed, and the patient had an excellent outcome with no wall motion abnormality.

Learning point: the prehospital ECG is critical, as was early prehospital cath lab activation. Were it not for this prehospital ECG and the cardiac arrest, the diagnosis may have been significantly delayed. Had this happened, the artery may have re-occluded prior to angiography, with resultant recurrent cardiac arrest and/or shock and death.

Friday, February 20, 2009

Here is a case of an 89 year old woman who had syncope but no chest pain or shortness of breath. Her initial EKG (#1) shows some nondiagnostic ST depression in V4-V6, probably due to LVH. She has a troponin of 0.13 ng/ml (ref range up to 0.09).

(#1)

She is admitted, her trop peaks at 0.23, her next day EKG done 8 hours later is shown below (#2) and shows some terminal T inversion in V3, consistent with the positive trop and suggesting tight LAD occlusion but open artery (T inversions are "reperfusion T waves; an inverted T wave is a sign of an open artery and an upright T wave is a sign of occlusion or re-occlusion). Echo the next day is normal. She is diagnosed with "demand ischemia" and discharged home.

(#2)

The patient returned with another episode of syncope 15 days later. She had no other symptom except weakness; none whatsoever. She had the following EKG at 0700:

(#3)

Here there is 4 mm of ST elevation that can only be due to myocardial ischemia. If there is any doubt, then the presence of new ST elevation and T inversion in I and aVL should erase that. If there is still any doubt, the loss of R-wave amplitude in V2 and V3 should erase that as well. The inversion of the T wave in aVL and V2 suggests an open artery. However, this is a very strange looking Wellens' T wave because of the marked ST elevation.

The treating physician contacted the cardiologist immediately, but the cardiologist was not convinced, mostly because of the minimal symptoms and partly because it is not the classic morphology of anterior STEMI due to persistently occluded LAD, which should have upright T waves.

So they recorded another EKG at 0720:

(#4)

Now the ST elevation is unmistakable, even with the persistently inverted T waves. But because the patient was asymptomatic, the cath lab was not yet activated. A bedside echo suggested anterior wall motion abnormality.

Another EKG was done at 0739:

(#5)

This shows even more ST elevation. The patient was still asymptomatic. An initial troponin returned at 12 ng/ml. The cath lab was activated. There was a ruptured plaque with thrombus in the LAD, with some flow still (accounting for the inverted T waves).

The following is a perfect example of Anterior MI with LAD occlusion but WITHOUT any ST elevation. This is seen commonly, but only recently reported on by de Winter, Verouden, Wilde, and Wellens' in a long letter to the New England Journal (NEJM 359(19):2071-2073; Nov. 6, 2008).

The authors reported this morphology in 2% of LAD occlusions. The morphology is as follows: 1-3 mm of upsloping ST depression in leads V1 to V6 that continues into tall, positive symmetrical T waves, with normal QRS and loss of R-wave progression and with 1-2 mm ST elevation in aVR. Interestingly, they found that this was not a transient feature that later progressed to ST elevation, but that it remained static until angiography up to 50 minutes after the initial ECG. The mean time from symptom onset was 90 minutes. K levels were normal. MI was very large as measured by high CK-MB.

This is the EKG of a previously healthy 40 year old man with one hour of chest pain and profound weakness and sense of "doom". He has a history of HTN, smoking, and family history. Vital signs and exam were normal.

This ECG show large symmetric T waves, best distinguished from those of early repolarization by the absence of large R-waves (in this case, the R-wave amplitude is very small). It also helps that there is inferior ST depression. There is some borderline ST elevation in leads V2 and V3. Similar to case 1, there is ST depression in leads V4-V6. This should be recognized as an EKG diagnostic for LAD occlusion.

A prehospital EKG had been done and is shown below (but has very poor quality)

This shows much ST elevation in anterior leads and illustrates an underrecognized phenomenon: hyperacute T waves are not only present early after occlusion, as the STEMI is developing, but also after the ST segment elevates AND they are present early after reperfusion as the ST segments are falling. They may be the only remaining clue to a reperfused LAD occlusion.

Case 3 (Hyperacute T waves misdiagnosed as Hyperkalemia).

49 yo man with 1 week of stuttering chest burning and tightness for 1-2 hours. Today the discomfort is associated with multiple episodes of vomiting and it is unremittant. The following EKG was obtained and hyperkalemia was diagnosed. The patient was treated with Calcium, Insulin, D50, and bicarbonate, with no change in the ECG. A bedside ultrasound revealed a possible anterior wall motion abnormality. The K returned at 2.9 mEq/L. There was an LAD occlusion that was opened and stented.

These T waves are NOT typical for hyperK. They are "fat" and wide, with a blunt peak and poor R-wave progression (especially V3). The T-waves of hyperkalemia are peaked and tented. See below:

Disclaimer

Cases come from all over the world. Patient identifiers have been redacted or patient consent has been obtained. The contents of this site have not been reviewed nor approved by Hennepin County Medical Center and any views or opinions expressed herein do not necessarily reflect the views or opinions of Hennepin County Medical Center.